Fernando P. Monroy

E-mail Dr. Monroy at Fernando.Monroy@nau.edu

BIO205--General Microbiology
BIO401--Immunobiology
BIO697--Seminar in Microbiology/Immunology
BIO698--Medical & Veterinary Parasitology

Immunoparasitology: immunobiology of host-parasite relationships
  Ph.D., University of Queensland, Australia
  Assistant Professor - Indiana State University (1993-1999)
  Associate Professor - Indiana State University (1999-2000)
  Joined the Department in 2000

     Research conducted by Dr. Monroy’s is directed towards clarification of the mechanisms employed by parasites to survive and establish successful infections. More specifically, I am interested in a group of parasitic organisms, the protozoa which includes the agents of such terrible diseases as malaria, leishmaniasis, toxoplasmosis and Chagas disease.
      My research interest involves the role of physiological stress in the pathogenesis of the obligated intracellular parasite Toxoplasma gondii. Stress in its wider interpretation, is a process central to the relationship between behavior and health. The physiological responses to stress are mediated through neural and endocrine systems. The two most likely routes by which the nervous system may communicate with cells of the immune system is by release of catecholamines from the sympathetic nervous system, and by secretion of glucocorticoid hormones following stimulation of the hypothalamic-pituitary-adrenal axis. My research goal intends to study the interactions between the nervous, endocrine and immune systems by using an infectious agent as a marker. The obligated intracellular parasite T. gondii is been used for two reasons: first, to investigate the effects of stress as a cofactor in the pathogenesis of an opportunistic infection in which cell-mediated immunity is of critical importance in host defense. Second, T. gondii is the most common opportunistic infectious agent of the central nervous system in HIV patients. Our interests center on the effects of stress in the modulation of regulatory cytokines [interferon (INF)-g , tumor necrosis factor (TNF)-a , interleukin (IL)-12 and IL-10] and neurohormones (glucocorticoids and catecholamine) in both the acute and chronic phases of T. gondii infection.

            LIFE CYCLE OF Toxoplasma gondii
    Secondly, I am interested in the role of catecholamines (Epinephrine and nor-Epinephrine) as immune modulators in protozoan infection.  My current research centers in the initial interaction of the parasite with the intestinal environment. During peroral infection with Toxoplasma gondii, IFN-g is required for survival in resistant strains (BALB/c); but in genetically susceptible mice (C57BL/6) IFN-g contributes to their early mortality. Mortality is associated with massive necrosis of the villi and mucosal cells in the ilea ofC57BL/6 mice within 7 days. These histologic changesare mediated by CD4+ T cells.  It is clear that local regulation of IFN-g following peroral infection is critical to determine whether this cytokine is protective or detrimental and to determine genetic resistance/susceptibility of the host to infection.  Our laboratory evaluates the effects of stress in an animal model of infections in which cell mediated immunity is known to be of primary importance in host defense.  Our studies integrate the effects of a physical stressor, cold water stress (CWS); manipulation of the the autonomic nervous system; T. gondii, a ubiquitous protozoan parasite; and the natural route of infection (peroral).  Using this mild physical stressor my laboratory has studied its effects in this host-parasite interaction during the acute phase after intraperitoneal (i.p.) and peroral infection.  CWS is detrimental to mice following i.p. infection, but beneficial during peroral infection.  We have

    NEURO-ADRENO-IMMUNE                    MACROPHAGES FROM STRESSED
            INTERACTIONS                                         (above) AND CONTROL MICE.

determined the effects of CWS on macrophage function (phagocytosis, nitric oxide production, etc) and activation (calcium mobilization). Our long-term goal is to understand the contribution of stress or stress-induced products to the outcome of infection in the intestinal environment. Intestines are heavily innervated by sympathetic fibers and local secretion of neurotransmitters (nor-epinephrine) is likely to affect the local environment and subsequent immune responses.  Our studies will investigate the contribution of nor-epinephrine to the observed regulation of intraepithelial and lamina propia lymphocytes during T. gondii infection.
 

Selected Publications:
MONROY, G.F. & ENRIQUEZ, F.J. (1992). Nematospiroides dubius as a model for chronic  intestinal parasitism.
    Review Article  for Parasitology Today, 8(2): 14-17.
MONROY, G.F. & LOKER, E.S. (1993). Production of heterogenous carbohydrate-binding proteins by the host snail
    Biomphalaria glabrata following exposure to Echinostoma paraensei and Schistosoma mansoni.Journal of
    Parasitology, 79: 416-421.
MONROY, G.F. & DRESDEN, M.H. (1996). Developmental expression and role of cysteine proteinases in
    Schistosoma  mansoni.International Journal for Parasitology, 25: 109-114.
MONROY, F.P. & DUSANIC, D.G. (1997). Mechanisms of survival of Trypanosoma musculi in the kidneys of
    chronically infected mice: kidney form reproduction and immunological reactions. Journal of Parasitology,
    83:848-852.
MONROY, F.P., MINNING, T. & DUSANIC, D.G. (1998). Trypanosoma musculi survival in the kidneys of
    chronically infected mice: kidney form ultrastructure , surface characteristics and serological interactions. Journal
    of  Parasitology, 84: 914-919.
BANERJEE, S., AVILES, H., FOX, M.T. & MONROY, F. (1999). Cold stress-induced modulation of cell immunity
    during acute Toxoplasma gondii infection in mice. Journal of Parasitology, 85: 123-132.
AVILES, H., BELLI, A., ARMIJOS, R., HARRIS, E. & MONROY, F.P. (1999). PCR detection and identification of
    Leishmania parasites in clinical specimens in Ecuador: a comparison with classical diagnostic methods. Journal
    of  Parasitology, 85: 147-153.
MONROY, F., BANERJEE, S., DUONG, P. & AVILES, H. (1999). Cold stress-induced modulation of inflammatory
    responses and  intra cerebral cytokine mRNA expression in acute murine toxoplasmosis. Journal of Parasitology,
    85: 878-896..
MONROY, F.P. & DUSANIC, D.G. (2000). The role of sequestered parasites in chronic infections. Review article for
    Parasitology Today, 16: 107-110.
AVILES, H. & MONROY, F. (2001). Immunomodulatory effects of cold stress on mice infected intraperitoneally with
    a lethal dose 50 (LD50) of Toxoplasma gondiiNeuroImmunomodulation,  9: 6-13.
MORDUE, D.G., MONROY, F.P., LA REGINA, M., SCHREIBER, R., DINARELLO, C. & SIBLEY, D. (2001). Acute
    toxoplasmosis leads to overproduction of Th1 cytokines. Journal of Immunology, 167:4574-4584.
AVILES, H. & MONROY, F. (2001).  Toxoplasma gondii: Cold stress-induced modulation of antibody responses.
    Experimental Parasitology, 99: 89-96.
GETZ, J. & MONROY, F. (2003). Effects of ?-and ?-adrenergic agonists on Toxoplasma gondii infection in murine
     macrophages. Journal of Parasitology. (in press).
AVILES, H., JOHNSON, M.T. & MONROY, F. (2003). Effects of cold stress on spleen cell proliferation and cytokine
    production during chronic Toxoplasma gondii infection. NeuroImmunomodulation. (in press).


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last modified May 1, 2003
Fernando Monroy